AB1050 THE LEVELS OF FECAL CALPROTECTIN, SERUM INTERLEUKIN 17/23, MALONDIALDEHYDE, GLUTATHIONE PEROXIDASE IN THE PATIENTS WITH AXIAL SPONDYLOARTHRITIS AND THEIR CORRELATIONS WITH CLINICAL, LABORATORY PARAMETERS, DISEASE ACTIVITY SCALES
Authors: M. Soysal, Ş. Kutlay, E. Devrim, Ç. Fidan, D. Gökmen, P. Yalçin
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Recent studies in the literature show that the fCal, some proinflammatory cytokines, oxidant/antioxidant markers are associated with disease activity in SpA(1,2,3). <h3>Objectives</h3> The aim of this study was to compare the levels of fCal, serum IL-17/23, malondialdehyde (MDA) and glutathione peroxidase (GPx) between the patients with axSpA treated with NSAID or anti-TNF and the control group; to evaluate the correlations of them with laboratory, clinical parameters, and disease activity scales. <h3>Methods</h3> 75 people from the outpatient clinic at Department of PMR Rheumatology Department, Ankara University were included in this cross-sectional study. Patients have met the ASAS classification criteria for axSpA. 25 volunteers participated in per group (NSAID group/anti-TNF group/the control group). The study was approved by the Clinical Research Ethics Committee, and all participants signed an informed consent form. Individuals participating in the study were evaluated with disease activity scales, ESR, and CRP. Via ELISA method, fCal level from stool samples and IL-17/23 level from serum samples; and via spectrophotometric method, the levels of MDA and GPx were measured. <h3>Results</h3> Fecal calprotectin level was found to be higher in the NSAID group than in anti-TNF group and to be at the lowest level in the control group, which is not statistically significant (p=0.05). In the anti-TNF group, the level of IL-23 is higher than that of the NSAID group (p=0.000). A weak positive correlation was detected between CRP and fCal level in the axSpA group (p=0.009/r=0.380). No relationship between fCal and disease activity scales was observed. It was detected that IL-17 has a weak positive correlation with BASDAI, ASDAS-CRP (p=0.035/r=0.311) and has a strong positive correlation with MASES (p=0.000/r=0.794). No relationship between IL-23 and disease activity scales was found. A weak positive correlation of MDA with BASFI and BASDAI was detected (p=0,018/r=0,355) (p=0,002/r=0,452). It was found a weak negative correlation between IL-23 and GPx (p=0,000/r=0,499), however no statistically significant relationship between the other levels was observed. <h3>Conclusion</h3> The fact that fCal level in the NSAID group is higher than the anti-TNF Group supports the literature that NSAIDs cause leaky gut syndrome by adversely affecting the gut microbiota. Higher fCal level in the NSAID group makes us think that in addition to intestinal inflammation caused by the disease, it is originated by the NSAID treatment[1]. In our study, the reason why the level of IL-23 in the NSAID group is lower may be the underlying mechanism through PGE2, and the reason why it is higher in the anti-TNF group may be that anti-TNF treatment has not had enough effect on the IL-17/23 pathway[2,4]. Especially the relationship of IL-17 level with MASES using for the clinical evaluation of the enthesitis areas, clinically shows us the role of the IL-17/23 pathway in the entheseal inflammation as well[5]. <h3>References</h3> [1]Klingberg, E., et al. (2017). "A longitudinal study of fecal calprotectin and the development of inflammatory bowel disease in ankylosing spondylitis." Arthritis Res Ther 19(1): 21. [2]Deveci, H., et al. (2019). "Serum Interleukin-23/17 Levels in Ankylosing Spondylitis Patients Treated with Nonsteroidal Anti-Inflammatory Drugs: A Prospective Cohort Study." J Interferon Cytokine Res 39(9): 572-576. [3]Ozgocmen, S., et al. (2004). "Serum nitric oxide, catalase, superoxide dismutase, and malondialdehyde status in patients with ankylosing spondylitis." Rheumatol Int 24(2): 80-83. [4]Milanez, F. M., et al. (2016). "IL-23/Th17 axis is not influenced by TNF-blocking agents in ankylosing spondylitis patients." Arthritis Res Ther 18: 52. [5]Schett G., et al., Enthesitis: from pathophysiology to treatment. Nat Rev Rheumatol. 2017; 21; 13(12): 731-41. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.